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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
Posted by Sherry on February 20, 2001, at 18:57:29
Hi All,
I have been diagnosed with adrenal insufficiency, and I suffer from atypical depression. I also, suffer from ferocious mood swings because of blood sugar fluctuations. Does anyone know why the adrenals are underactive in atypical depression, and overactive in typical depression? I found the article below, and it piqued my curiousity.
Sherry
Prednisone augmentation in treatment-resistant depression with fatigue and hypocortisolaemia: a case series
Bouwer C, Claassen J, Dinan TG, Nemeroff CB
Department of Psychological Medicine, University of Otago University, Dunedin, New Zealand. colin.bouwer@stonebow.otago.ac.nz
[Record supplied by publisher]
Abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis have long been implicated in major depression with hypercortisolaemia reported in typical depression and hypocortisolaemia in some studies of atypical depression. We report on the use of prednisone in treatment-resistant depressed patients with reduced plasma cortisol concentrations. Six patients with treatment-resistant major depression were found to complain of severe fatigue, consistent with major depression, atypical subtype, and to demonstrate low plasma cortisol levels. Prednisone 7.5 mg daily was added to the antidepressant regime. Five of six patients demonstrated significant improvement in depression on prednisone augmentation of antidepressant therapy. Although hypercortisolaemia has been implicated in some patients with depression, our findings suggest that hypocortisolaemia may also play a role in some subtypes of this disorder. In treatment-resistant depressed patients with fatigue and hypocortisolaemia, prednisone augmentation may be useful.
PMID: 10999245
--------------------------------------------------------------------------------
Posted by Bradley on February 20, 2001, at 20:34:24
In reply to hypocortisolaemia and hypercortisolaemia , posted by Sherry on February 20, 2001, at 18:57:29
I suffer from atypical depression and have hypercortisolaemia. Just opposite of the study.
I sure have heard many horror stories about prednisone. Can't say I would'nt try a treatment with it, but I would be scared.> Hi All,
>
> I have been diagnosed with adrenal insufficiency, and I suffer from atypical depression. I also, suffer from ferocious mood swings because of blood sugar fluctuations. Does anyone know why the adrenals are underactive in atypical depression, and overactive in typical depression? I found the article below, and it piqued my curiousity.
>
> Sherry
>
> Prednisone augmentation in treatment-resistant depression with fatigue and hypocortisolaemia: a case series
>
> Bouwer C, Claassen J, Dinan TG, Nemeroff CB
>
> Department of Psychological Medicine, University of Otago University, Dunedin, New Zealand. colin.bouwer@stonebow.otago.ac.nz
>
> [Record supplied by publisher]
>
> Abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis have long been implicated in major depression with hypercortisolaemia reported in typical depression and hypocortisolaemia in some studies of atypical depression. We report on the use of prednisone in treatment-resistant depressed patients with reduced plasma cortisol concentrations. Six patients with treatment-resistant major depression were found to complain of severe fatigue, consistent with major depression, atypical subtype, and to demonstrate low plasma cortisol levels. Prednisone 7.5 mg daily was added to the antidepressant regime. Five of six patients demonstrated significant improvement in depression on prednisone augmentation of antidepressant therapy. Although hypercortisolaemia has been implicated in some patients with depression, our findings suggest that hypocortisolaemia may also play a role in some subtypes of this disorder. In treatment-resistant depressed patients with fatigue and hypocortisolaemia, prednisone augmentation may be useful.
>
> PMID: 10999245
>
> --------------------------------------------------------------------------------
Posted by JohnX on February 21, 2001, at 3:53:00
In reply to This theory is reversed for me, posted by Bradley on February 20, 2001, at 20:34:24
Sherry/Bradley,
Crack open some Provigil (narcolespy med) to
read this.Hypercortisolemia is often spotted as a marker for
many depressives. I don't believe their is
much of any difference here between atypical or
typical depression. Someone can correct me if I'm
wrong.There are receptors in the brain called
corticosteriod receptors (I'll call this "CR")
that act in response to cortisol (steroids like
dexamethasone can emulate cortisol). Disruptions
in the CRs often occur during episodes of depression.
This is related to disruptions in what is called
the HPA (Hypthalamus-Pituitary-Adrenal gland)
axis (fancy scientific mumbo-jumbo). Alterations
in CRs can occur as a result of Hyperactivity of
the HPA axis or a primary defect of the
receptors themselves. The Adrenal gland is
responsible for the release of adrenocortisol.From what I know, here is generally what is seen in most depressives who have functionally healthy
HPA encodrines but show hypercortisolemia:Alterations in the CRs (like their sensitivity
to cortisol) occur as a result of hyperactivity
of the HPA axis or a primary defect resulting in abnormal CRs sensitivity to cortisol.
In the 1st case, generally the CRs are "down-regulated" (made less sensitive). This can occur
for example during excessive chronic stress which
continually releases cortisol causing the CRs to
down regulate. There could be other reasons too
(I'm not a guru on this). In the 2nd case,
primary dysfunction some inherint defect in the
CR cells themselves causes the problem (I believe
this is less common).
Activation of CRs ultimately causes activation
of a feedback mechanism that stops cortisol
release. If the CRs are overly down regulated,
then the feedback mechanism is disrupted and the body continues to release cortisol, leading to
hypercortisolemia. Somehow the CRs are involved
in other brain activity which correlates to
the depression. Chronic anti-depressant admin has
been shown to normalize the Crs sensitivity, thus
fixing the dysfunctional feedback system (hypo-supression
of the negative feedback). There's actually
a test to verify this where a steroid such
as dexamethasone is injected and the base
line cortisol level doesn't drop as much
as inticipated.In hypocortisolemia the opposite can occur.
This is less common. *Really* chronic stress or
traumatic episodes may contribute to Adrenal
insufficiency. There are also many other medical
reasons (disease or what not) too.
Since the Adrenal glands produce adreno-cortisol
but the Adrenal glands are impaired,
the baseline cortisol levels are chronically low
causing the CRs to up-regulate (increased sensitivity). This may lead to hypo-surpression
in the feedback loop. The up-regulation of the
CRs can also impact brain activity in a way that
causes depression. These patients probably need
to receive steroid injections in order to correct
the problem. Any comments Shirly?Anyways, that's what I've read.
-John
> >
> > Sherry
> >
> > Prednisone augmentation in treatment-resistant depression with fatigue and hypocortisolaemia: a case series
> >
> > Bouwer C, Claassen J, Dinan TG, Nemeroff CB
> >
> > Department of Psychological Medicine, University of Otago University, Dunedin, New Zealand. colin.bouwer@stonebow.otago.ac.nz
> >
> > [Record supplied by publisher]
> >
> > Abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis have long been implicated in major depression with hypercortisolaemia reported in typical depression and hypocortisolaemia in some studies of atypical depression. We report on the use of prednisone in treatment-resistant depressed patients with reduced plasma cortisol concentrations. Six patients with treatment-resistant major depression were found to complain of severe fatigue, consistent with major depression, atypical subtype, and to demonstrate low plasma cortisol levels. Prednisone 7.5 mg daily was added to the antidepressant regime. Five of six patients demonstrated significant improvement in depression on prednisone augmentation of antidepressant therapy. Although hypercortisolaemia has been implicated in some patients with depression, our findings suggest that hypocortisolaemia may also play a role in some subtypes of this disorder. In treatment-resistant depressed patients with fatigue and hypocortisolaemia, prednisone augmentation may be useful.
> >
> > PMID: 10999245
> >
> > --------------------------------------------------------------------------------
Posted by JohnX on February 21, 2001, at 3:58:39
In reply to Re: This theory is reversed for me, posted by JohnX on February 21, 2001, at 3:53:00
Oops, typo. In the hypocotisolemia case there
is hyper-supression of cortisol in the feedback
loop not hypo-surpression.
> In hypocortisolemia the opposite can occur.
> This is less common. *Really* chronic stress or
> traumatic episodes may contribute to Adrenal
> insufficiency. There are also many other medical
> reasons (disease or what not) too.
> Since the Adrenal glands produce adreno-cortisol
> but the Adrenal glands are impaired,
> the baseline cortisol levels are chronically low
> causing the CRs to up-regulate (increased sensitivity). This may lead to hypo-surpression
> in the feedback loop. The up-regulation of the
> CRs can also impact brain activity in a way that
> causes depression. These patients probably need
> to receive steroid injections in order to correct
> the problem. Any comments Shirly?
>
> Anyways, that's what I've read.
>
> -John
>
>
>
>
> > >
> > > Sherry
> > >
> > > Prednisone augmentation in treatment-resistant depression with fatigue and hypocortisolaemia: a case series
> > >
> > > Bouwer C, Claassen J, Dinan TG, Nemeroff CB
> > >
> > > Department of Psychological Medicine, University of Otago University, Dunedin, New Zealand. colin.bouwer@stonebow.otago.ac.nz
> > >
> > > [Record supplied by publisher]
> > >
> > > Abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis have long been implicated in major depression with hypercortisolaemia reported in typical depression and hypocortisolaemia in some studies of atypical depression. We report on the use of prednisone in treatment-resistant depressed patients with reduced plasma cortisol concentrations. Six patients with treatment-resistant major depression were found to complain of severe fatigue, consistent with major depression, atypical subtype, and to demonstrate low plasma cortisol levels. Prednisone 7.5 mg daily was added to the antidepressant regime. Five of six patients demonstrated significant improvement in depression on prednisone augmentation of antidepressant therapy. Although hypercortisolaemia has been implicated in some patients with depression, our findings suggest that hypocortisolaemia may also play a role in some subtypes of this disorder. In treatment-resistant depressed patients with fatigue and hypocortisolaemia, prednisone augmentation may be useful.
> > >
> > > PMID: 10999245
> > >
> > > --------------------------------------------------------------------------------
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Dr. Bob is Robert Hsiung, MD,
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